Department of Structural Biology, Stanford University School of Medicine, Stanford, CA 94305, USA; Program in Biophysics, Stanford University, Stanford, CA 94305, USA.
Department of Structural Biology, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Applied Physics, Stanford University, Stanford, CA 94305, USA.
J Mol Biol. 2020 Jul 24;432(16):4499-4522. doi: 10.1016/j.jmb.2020.06.003. Epub 2020 Jun 6.
A hallmark of the initiation step of HIV-1 reverse transcription, in which viral RNA genome is converted into double-stranded DNA, is that it is slow and non-processive. Biochemical studies have identified specific sites along the viral RNA genomic template in which reverse transcriptase (RT) stalls. These stalling points, which occur after the addition of three and five template dNTPs, may serve as checkpoints to regulate the precise timing of HIV-1 reverse transcription following viral entry. Structural studies of reverse transcriptase initiation complexes (RTICs) have revealed unique conformations that may explain the slow rate of incorporation; however, questions remain about the temporal evolution of the complex and features that contribute to strong pausing during initiation. Here we present cryo-electron microscopy and single-molecule characterization of an RTIC after three rounds of dNTP incorporation (+3), the first major pausing point during reverse transcription initiation. Cryo-electron microscopy structures of a +3 extended RTIC reveal conformational heterogeneity within the RTIC core. Three distinct conformations were identified, two of which adopt unique, likely off-pathway, intermediates in the canonical polymerization cycle. Single-molecule Förster resonance energy transfer experiments confirm that the +3 RTIC is more structurally dynamic than earlier-stage RTICs. These alternative conformations were selectively disrupted through structure-guided point mutations to shift single-molecule Förster resonance energy transfer populations back toward the on-pathway conformation. Our results support the hypothesis that conformational heterogeneity within the HIV-1 RTIC during pausing serves as an additional means of regulating HIV-1 replication.
HIV-1 逆转录起始步骤的一个标志是,病毒 RNA 基因组被转化为双链 DNA,其特点是速度慢且非连续性。生化研究已经确定了病毒 RNA 基因组模板上的特定位置,逆转录酶 (RT) 在这些位置停滞。这些停滞点发生在添加三个和五个模板 dNTP 之后,可能作为检查点,以调节病毒进入后 HIV-1 逆转录的精确时间。逆转录酶起始复合物 (RTIC) 的结构研究揭示了独特的构象,这些构象可能解释了掺入的缓慢速率;然而,关于复合物的时间演变和在起始过程中导致强烈暂停的特征仍存在疑问。在这里,我们展示了在三轮 dNTP 掺入 (+3) 后 RTIC 的低温电子显微镜和单分子特征,这是逆转录起始过程中的第一个主要暂停点。+3 延伸 RTIC 的低温电子显微镜结构揭示了 RTIC 核心内的构象异质性。鉴定出三种不同的构象,其中两种采用独特的、可能偏离通路的中间产物,处于典型的聚合循环中。单分子Förster 共振能量转移实验证实,+3 RTIC 比早期 RTIC 更具结构动态性。通过结构导向的点突变选择性破坏这些替代构象,将单分子Förster 共振能量转移群体转移回通路构象。我们的结果支持这样的假设,即在 HIV-1 RTIC 中,暂停时的构象异质性是调节 HIV-1 复制的另一种手段。